Fibrosis can be generally defined as excessive deposition of extra cellular matrix (ECM) components such as fibronectin (FN) and type I collagen (Col1α1) by organ fibroblasts. Organ fibrosis is the final common pathway for many diseases that result in end-stage organ failure. However, effective therapy for organ fibrosis is unavailable. Uncontrollable wound-healing responses, including acute and chronic inflammation, angiogenesis, activation of resident cells, and ECM remodeling, are thought to be involved in the pathogenesis of fibrosis. TGF-β is a prototype fibrotic cytokine that is increased in fibrotic organs and contributes to the development of fibrosis by stimulating the synthesis of ECM molecules, activating fibroblasts to α smooth muscle actin (α SMA)-expressing myofibroblasts, and downregulating matrix metalloproteinases (MMPs). However, a clinical trial of a monoclonal anti-TGF-β antibody in fibrosis patients, such as those with early secondary sclerosis (SSc), failed to show any efficacy (Varga and Pasche, Nature Reviews Rheumatology 2009; 5:200-6).